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Abstract Background and purpose: Recent studies showed that erythropoietin (EPO) despite having role in hematopoiesis, has non-hematopoietic tissue protective effects on ischemia-reperfusion injury. In this study we evaluated the effects of erythropoietin on reducing ischemia-reperfusion injuries after coronary artery bypass graft surgery (CABG). Materials and methods: 60 patients that was candidate for elective CABG randomly divided into two groups, EPO and control group. Patients in EPO group received IV infusion of EPO (700 IU/kg), at the start of reperfusion after aorta cross clamp. Cardiac markers: Troponin I and Creatine kinase MB (CKMB) assessed 8hours after CABG surgery. Also echocardiography was performed in all patients 6month after surgery. Results: Troponin I level had no difference in EPO and control group (P=0.30). CKMB level in EPO group was higher than control group (P=0.004). After 6month from surgery, Ejection fraction (EF) in EPO group was higher than control group but differences wasn’t significant (P=0.46). But Left ventricle end systolic diameter (P=0.017) and also Left ventricle end diastolic diameter (P= 0.04) in EPO group were significantly lesser than control group 6month after surgery Conclusion: in this study the administration of erythropoietin was associated with reduction in ischemia-reperfusion injuries by improving ventricular function, and also with reduction in myocardial remodeling and decrease in Left ventricle end systolic diameter and Left ventricle end diastolic diameter

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Background and purpose: Vitamin C and CoQ10 are known as two potentantioxidants. We studied the protective Role of CoQ10 and ascorbic acid against Ischemia-Reperfusion. Finally, we have compared the therapeutic effect of these two together. Materials and methods: 35 male balb-Cwere divided into seven subgroups. Includes five groups: intact, ischemicControl, sham Control and treatment groups with CoQ10 and treatment groups with ascorbic acid. In treatment groups, the mice treated with CoQ10 and vitC as Pre-Treatment for a week. Then, ischemia induced by Common Carotid artery ligation. The mice post-treated with CoQ10and ascorbic acidfor a week. Nissl staining applied to counting necroticCells of hippocampus. TUNNEL kit was used to quantify apoptoticCell death while to short term memory scale, we apply y-maze and shuttle box tests. Results: High rate of apoptosis was seen in ischemic group associated with significantly short-term memory loss. In the treatment groups withthese antioxidants, Cell death was significantly lower than the ischemic Control group. Between treatment groups, group treated with CoQ10 was less neuronal death than the group treated with ascorbic acid. Conclusion: According to the results of this study, ascorbic acid and CoQ10 intake significantly reduced Cell death and decreased memory loss. Butthe antioxidant effect of CoQ10 is stronger than vitamin C in this zone of brain.

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Background and purpose: Lavender is a medicinal plant with antioxidant activity. Stroke causes long term disability and is associated with oxidative stress. The present study was conducted to evaluate the protective effect of lavender extract against blood brain barrier permeability and its possible mechanisms in an experimental model of stroke. Materials and methods: In this experimental study, 42 male Wistar rats weighing 250 to 300 g were used. The rats were divided into 6 groups (n= 7 per group). Group 1 was ischemic, groups 2 and 3 were ischemic that were given 100 and 200 mg/kg lavender extract, respectively. Group 4 were intact and groups 5 and 6 were intact groups which received lavender extract with dose of 100 and 200 mg/kg. Group 7 was also considered as the sham. Focal cerebral ischemia was induced in rats by the transient occlusion of the middle cerebral artery for 1 hr. Data were analysed with SPSS and comparison of means were compared using One Way Anova. Results: The ethanolic extract of lavender at 200 mg/kg significantly reduced the blood brain barrier permeability in rat stroke model compared with ischemic group. Conclusion: The results indicate that lavender extract has neuroprotective activity against cerebral ischemia and alleviated neurological function in rats.

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Background and purpose: Damage caused by ischemia/reperfusion (I/R) is one of the major causes of liver failure during surgeries. Endothelin as the main vasoconstrictor has two receptors; ET_A and ET_B. Increased number of ET_B during ischemia-reperfusion, reduces tissue damages by sinusoidal dilation. This study investigated the effects of dexamethasone against liver endothelial glycocalyx injury and ET_B receptor gene expression during hepatic ischemia/reperfusion in rats.

Materials and methods: Thirty two male Wistar rats were divided into four groups; a SHAM-operated group that received normal saline, DEX; which had dexamethasone injection (10 mg/kg), the I/R; received normal saline during ischemia/reperfusion, and the DEX + IR with I/R that received dexamethasone (10 mg/kg, 60 minutes before ischemia and immediately after reperfusion). After 1 hour of ischemia and 3 hours of reperfusion the blood samples and liver tissues were collected. The relative gene expression of ET_B was assessed by real time PCR. Serum samples were used to measure the level of ALT and AST and hyaluronic acid (HA).

Results: The level of ALT, AST and HA significantly increased in I/R compared with those of the SHAM-operated group (P<0.001). Injection of dexamethasone in the DEX+IR caused a significant reduction in serum indicators compared to those of the I/R group (P<0.001). Elevated ET_B receptor gene expression reduced by dexamethasone injection (P> 0.05).

Conclusion: Dexamethasone decreased ET_B receptor gene expression during liver I/R. In addition, it significantly protected the parenchymal cells and sinusoidal endothelial glycocalyx. Therefore, dexamethasone could play an important role in reducing liver injury during I/R.

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Background and purpose: Cerebral ischemia is a general injury characterized by direct tissue damage and increasing free radicals that leads to the death of brain tissue, cerebral infarction, or ischemic stroke. Some studies have demonstrated anti-inflammatory, antipyretic and antibacterial activities of Viola odorata. However, key aspects of the effect of Viola odorata in stroke are scarce. This study investigated the effect of Viola odorata extract (VOE) on neurological deficit scores (NDS) and infarct volume (IV) in MCAO stroke model.

Materials and methods: In this experimental study, 20 male Wistar rats weighing 200 to 300 g were assigned to 4 groups including three treatment groups and control group. After preparation of VOE, the experimental groups received different doses of VOE (25, 50 and 75 mg/kg) by gastric gavage while the control group received distilled water for 30 days by gastric gavage. Two hours after the last gavage, the rats were exposed to 60 min MCAO surgery and 24 hours later, the IV and NDS were evaluated.

Results: Compared with the control group, reduction was seen in total IV and NDS in animals treated with VOE50. Investigation of IV in the core, penumbra and subcortex of right hemisphere demonstrated that VOE25 and VOE50 decreased IV in the subcortex and core regions, and just VOE50 decreased IV in the penumbra during the treatment. VOE75 decreased IV only in the subcortex region.

Conclusion: Although further studies are needed to clarify the mechanism of Viola odorata, the present study explored the potential effect of Viola odorata extract on reducing infarct volume and neurological defects in MCAO stroke model. This study could be helpful for future exploration of protective effect of V. odorata on cerebral ischemia.

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Ischemia-reperfusion injuries (IRI) are the major causes of liver failure after various types of liver surgeries such as biopsy, transplantation, and tumor surgery. Its pathogenesis is multifactorial and complex that involves ATP depletion, hepatocyte edema, acidosis, oxidative stress, inflammation, and microcirculation defect which can eventually progress to liver cell death, systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome, and even acute graft rejection. There are much evidences that suggest applying anti-inflammatory drugs could be a proper strategy to decrease IRI. Dexamethasone is a highly potent synthetic corticosteroid that its beneficial effects on various tissues in IRI are well documented. It also suppresses inflammation and immune response in different pathologic conditions. Its functional mechanism is different in various types of cells and involves: inactivation of NF-κB and AP-1, inhibition of releasing PLA₂ and arachidonic acid, and induction of ERK1/2 and SGK-1. By these processes dexamethasone is able to prevent cytokine overproduction and leukocyte activation, recruitment and infiltration. In this review, we aimed to explain the protective effects of dexamethasone on liver ischemia-reperfusion injuries.
 

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Background and purpose: Ischemia-reperfusion injuries (I/RI) are the major causes of liver failure after various types of liver surgeries, particularly liver transplantation. Reactive oxygen species (ROS) are the major causes of such injuries, therefore, antioxidant therapy to attenuate hepatic lesions is preferred. We aimed to evaluate the effects of silibinin, a potent radical scavenger, on liver damages and endothelial and inducible nitric oxide synthase (eNOS and iNOS) genes expression after liver I/R.
Materials and methods: In this experimental study, the rats were divided into four groups (n=8 per group). Group1 Vehicle: the rats underwent laparotomy and received DMSO10%, Group 2 SILI: the animals received silibinin alongside laparotomy, Group3 I/R: the rats received DMSO10% and subjected to liver I/R procedure, and group 4 I/R+SILI: this group received both silibinin and liver I/R simultaneously. Silibinin (50 mg/kg I.P) was administered twice in all rats. After 1 h ischemia and 5 h reperfusion, blood samples were collected to evaluate serum AST and ALT levels and liver sections were taken to analyze the eNOS and iNOS gene expressions and histological examinations.
Results: There were no significant differences in all parameters between Vehicle and SILI groups (p>0.05). But serum AST and ALT increased significantly in I/R group compared with those in vehicle group. Treatment with silibinin could considerably reduce these markers. Histological damages during I/R improved by silibinin. The iNOS gene was found to be overexpressed whereas eNOS expression decreased in I/R group compared with those in the vehicle group. Silibinin treatment could decline iNOS expression but could not significantly affect eNOS expression (p>0.05).
Conclusion: Silibinin protects liver from I/RI. It may decrease iNOS adverse effects by suppressing its expression.

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Introduction: Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in women during reproductive ages. This syndrome is associated with disruption of sex hormone levels. Studies have shown that endurance of the heart to ischemia-reperfusion (I/R) injury can be affected by sex hormones. In the present study, the rate of cardiac tolerance against I/R injury in the PCOS rat model was compared with normal (control) rats.
Materials and Methods: The rats were randomly divided into two groups; PCOS and control (n=8 per group). The hearts were isolated in Langendorff isolated heart system. Cardiac perfusion was performed in a retrograde flow in the aorta at constant pressure (75 mmHg) by Krebs-Henslit buffer. A pressure (5-10 mmHg) was put to the left ventricle, using an intraventricular balloon, to measure the hemodynamic parameters of the heart. Cardiac signals were recorded while being transmitted through the catheter to the Powerbull system.
Results: Before I/R, the values for cardiac hemodynamic parameters including HR, LVDP, RPP and ± dp/dt, increased in the rat model of PCOS compared to controls, although these increases were not statistically significant (P>0.05). These parameters had decreasing trends after I/R in PCOS rats compared to controls which were not statistically significant (P>0.05).
Conclusion: Cardiac resistance to I/R injury was found to be similar in both PCOS and control animals, which could be due to the cardioprotective role of sex hormones such as estrogens.

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Background and purpose: The present study aimed at exploring the effects of eight-week high intensity interval training (HIIT) program on gene expression factors involved in cholesterol reverse transport in liver tissue of ischemic rats.
Materials and methods: In this study, 28 Wistar Rats (250 ±20 g) were randomly divided into four groups: Ischemia (n=8), Placebo (n=8), Training (n=8), and Ischemia plus Training (n=8). Myocardial infarction was induced by ligation of left anterior descending coronary artery (LAD) for 30 minutes. High intensity interval training program (4 min of running at 85-90% VO2max and 2 min active recovery at 50-60% VO2max) was performed using treadmill for 8 weeks (three times a week /40 minutes).
Results: The expression levels of ABCG1 receptor gene and Apolipoprotein A1 significantly increased in high intensity interval training group compared to Ischemia group (P=0.008) and placebo group (P= 0.037). Also, the expression of Apolipoprotein 2 receptor gene showed significant increase in HIIT+ Ischemia group compared to Ischemia group (P=0.041) and placebo group (P=0.04). In addition, the expression of SR-BR receptor gene was found to increase in HIIT+ Ischemia group compared to the placebo group (P=0.028).
Conclusion: High intensity interval training in ischemic rats increases the key factors involved in reverse cholesterol transfer process and ultimately leads to an increase in HDL, which has a positive effect on prevention of atherosclerosis and ischemia.